SAT-172 - Adult-Onset Idiopathic Hypogonadotropic Hypogonadism Presenting with Profound Testosterone Deficiency in A Middle-Aged Man

Background: Adult-onset idiopathic hypogonadotropic hypogonadism (AO-IHH) is a rare and underrecognized disorder characterized by acquired gonadotropin deficiency after normal pubertal development, in the absence of identifiable structural, systemic, or functional causes.

Clinical

Case: A 55-year-old man with hypertension and dyslipidemia presented with progressive fatigue, dizziness, headaches, and loss of spontaneous morning erections since 2020. He reported normal puberty at age 13, preserved libido until symptom onset, intact olfaction, and prior fertility with four healthy sons. He denied head trauma, exogenous androgen exposure, substance use, testicular injury, infections, infiltrative disease, or family history of endocrine disorders. Brain MRI with pituitary protocol demonstrated a normal pituitary gland. Physical examination revealed preserved facial hair, diminished skeletal muscle mass, increased abdominal adiposity, absence of gynecomastia, normal testicular size, and a BMI of 26.3 kg/m2. Initial fasting morning total testosterone was profoundly low at 4.53 ng/dL (193–836), confirmed on repeat testing at 8.64 ng/dL with inappropriately low LH 1.15 mIU/mL (1.7–8.6) and FSH 1.22 mIU/mL (1.5–12.4). Hemoglobin levels were mildly low at 13.30 g/dL (14.0-18.0). Prolactin, thyroid function, IGF-1, iron indices, cortisol, renal function, electrolytes, and glucose were normal; infectious and toxicology screening were negative. DXA revealed osteopenia with a lowest T-score of −1.5 at the right femur. Based on acquired severe hypogonadotropic hypogonadism following normal puberty and fertility, normal pituitary imaging, and exclusion of secondary causes, a diagnosis of AO-IHH was established. After evaluation of PSA levels, the patient was initiated on intramuscular testosterone cypionate and dose will be gradually titrated. He will be followed for signs of clinical improvement, along with serial monitoring of serum testosterone, hematocrit, PSA, and metabolic parameters.

Conclusion: This case highlights AO-IHH as a distinct and treatable cause of acquired male hypogonadism that may present decades after normal pubertal development and fertility. Recognition is essential to prevent long-term complications such as bone loss, anemia, and impaired quality of life. Increasing awareness of AO-IHH is critical, as its nonspecific presentation frequently delays diagnosis.

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